ライフサイエンスコーパス: thiazide

1 and exhibited a severely blunted response to thiazide.

2 ith an increase in the natriuretic effect of thiazide.

3 orming cells may be an additional target for thiazides.

4 First, eel NCCbeta is resistant to thiazides.

5 nts; or 1.5% of the overall percentage using thiazides [33.4%], P = .01).

6 rinol combined with thiazide was superior to thiazide alone.

7 s lithium-NDI development in mice similar to thiazide/amiloride but with fewer adverse effects.

8 nt of lithium-NDI mice with acetazolamide or thiazide/amiloride induced similar antidiuresis and incr

9 Thiazide/amiloride-treated mice showed hyponatremia, hyp

10 a slight differential increase in the use of thiazides among beneficiaries with hypertension in the 2

11 ients with bipolar disorder are treated with thiazide and amiloride, which are thought to induce anti

12 erventions and more among those who received thiazide and citrate than among control patients.

13 Thiazide and loop diuretics were associated with higher

14 Thiazide and loop diuretics were associated with increas

15 Hypersensitivity to thiazide and loop diuretics, angiotensin-converting enzy

16 Use of diuretics (both thiazide and nonthiazide), activity levels and muscle st

17 e-affirms the initial ALLHAT conclusion that thiazide and similar diuretics (at evidence-based doses)

18 ronic kidney disease, selection and doses of thiazide and similar diuretics, and the association of a

19 Thiazide and thiazide-like diuretic agents are being inc

20 beta blockers) was significantly better than thiazides and thiazide-like diuretics as a first-line th

21 escribing combinations of potassium citrate, thiazides, and bisphosphonates, and correcting bone and

22 Thiazide-based treatment gives less cardiovascular prote

23 people similar to that in outcome trials of thiazide-based treatment.

24 2 different BP lowering-regimens (atenolol+/-thiazide-based versus amlodipine+/-perindopril-based the

25 nt classes of blood pressure-lowering drugs (thiazides, beta-blockers, ACE inhibitors, and angiotensi

26 However, the thiazide-binding site in NCC is unknown.

27 ing diuretic, amiloride, to treatment with a thiazide can prevent glucose intolerance and improve blo

28 th multiple past calcium stones, addition of thiazide, citrate, or allopurinol further reduced risk.

29 Its inhibition with thiazides constitutes the primary baseline therapy for a

30 tems, coexpression of NCC with I-1 increased thiazide-dependent Na(+) uptake, whereas RNAi-mediated k

31 Thiazides did not affect osteoblast proliferation, but d

32 New-onset diabetes associated with thiazides did not increase cardiovascular outcomes.

33 Overall, our study demonstrates that thiazides directly stimulate osteoblast differentiation

34 ihypertensive drug than in those receiving a thiazide diuretic (-2.38 mm Hg [-6.16 to 1.40]).

35 ny diuretic (HR 1.48 [95% CI 1.11, 1.98]), a thiazide diuretic (HR 1.44 [95% CI 1.00, 2.10]), or a lo

36 drug (NSAID; P = .03), statin (P = .01), and thiazide diuretic (P = .025) intake was inversely relate

37 The potency series of thiazide diuretic action (acetazolamide > chlorothiazide

38 should be given to medical treatment with a thiazide diuretic and/or citrate therapy.

39 ts were used to test the hypothesis that the thiazide diuretic chlorthalidone would decrease urine ca

40 Thiazide diuretic drugs act in the distal convoluted tub

41 However, although thiazide diuretic drugs have been advocated as first-lin

42 eabsorption mechanisms provides insight into thiazide diuretic efficacy.

43 The intact hypocalciuric response to a thiazide diuretic indicates that inactivation of the ClC

44 , continuous infusions, or the addition of a thiazide diuretic or aldosterone antagonist.

45 nd unravel a complex mechanism that explains thiazide diuretic resistance.

46 reasing diuretic dosage, concurrent use of a thiazide diuretic to inhibit downstream NaCl reabsorptio

47 pediatric patients indicate that citrate or thiazide diuretic treatment may improve BMD.

48 Five years of NSAID, statin, and thiazide diuretic use was associated with PSA levels low

49 nts with normal plasma K+ and aldosterone, a thiazide diuretic, bendroflumethiazide, would be as effe

50 recommends pharmacologic monotherapy with a thiazide diuretic, citrate, or allopurinol to prevent re

51 i-drug combination, particularly including a thiazide diuretic, is very often necessary and should be

52 red with not using any diuretic, not using a thiazide diuretic, or not using a loop diuretic, respect

53 than treatment with an ACE inhibitor plus a thiazide diuretic.

54 Thiazide diuretics (TD) are commonly prescribed anti-hyp

55 onstrating the efficacy of very low doses of thiazide diuretics added to other antihypertensive agent

56 Previous research has suggested that thiazide diuretics and beta-blockers may promote the dev

57 The studies most strongly support the use of thiazide diuretics and long-acting calcium channel block

58 n mechanisms and sites of action of loop and thiazide diuretics and the similarity of their chronic e

59 Thiazide diuretics are among the most commonly prescribe

60 As thiazide diuretics are among the most efficacious agents

61 Thiazide diuretics are among the most widely used treatm

62 essential hypertension remains unknown, but thiazide diuretics are frequently recommended as first-l

63 Thiazide diuretics are frequently used in these patients

64 the major conclusion of this trial was that thiazide diuretics are superior in preventing 1 or more

65 The initial ALLHAT conclusion, that thiazide diuretics are superior to angiotensin-convertin

66 Thiazide diuretics are used to treat hypertension; howev

67 Thiazide diuretics are used worldwide as a first-choice

68 scriptomics) to identify novel biomarkers of thiazide diuretics BP response.

69 suggests VASP as a potential determinant of thiazide diuretics BP response.

70 Thiazide diuretics have proven themselves effective agai

71 We found that men using NSAIDs, statins, and thiazide diuretics have reduced PSA levels by clinically

72 ciuric stones, sodium restriction along with thiazide diuretics helps to reduce urinary calcium.

73 ature evaluating the combination of loop and thiazide diuretics in patients with heart failure in ord

74 Potassium depletion by thiazide diuretics is associated with a rise in blood gl

75 suggest that inexpensive and well-tolerated thiazide diuretics may be especially effective in preven

76 directly in cells expressing NCC, indicating thiazide diuretics may be particularly effective for low

77 apy with beta-receptor blockers, digoxin and thiazide diuretics may worsen sexual dysfunction owing t

78 er exclusion of participants who were taking thiazide diuretics or those with diabetes.

79 The combination of statins and thiazide diuretics showed the greatest reduction in PSA

80 d not discourage physicians from prescribing thiazide diuretics to nondiabetic adults who have hypert

81 Thiazide diuretics treat the disease, fostering the view

82 with blood pressure less than 140/90 mm Hg; thiazide diuretics used in multidrug hypertensive regime

83 , subjects with hypertension who were taking thiazide diuretics were not at greater risk for the subs

84 Loop or thiazide diuretics were used in all 14 patients, and ang

85 open-label antihypertensive therapy (mostly thiazide diuretics) added as needed to control blood pre

86 serotonin reuptake inhibitors, statins, and thiazide diuretics), with evaluation of how often drugs

87 Thiazide diuretics, ACE-inhibitors or angiotensin recept

88 ce of PHAII phenotypes, their sensitivity to thiazide diuretics, and the observation that they consti

89 Thiazide diuretics, angiotensin II receptor blockers, an

90 However, it is reasonable to conclude that thiazide diuretics, angiotensin-II receptor blockers, an

91 Overall, the use of thiazide diuretics, beta-blockers, angiotensin-convertin

92 otensin II receptor blockers, beta-blockers, thiazide diuretics, calcium channel blockers, and metfor

93 Thiazide diuretics, niacin, and beta-adrenergic blockers

94 patients with truly resistant hypertension, thiazide diuretics, particularly chlorthalidone, should

95 l nephron of the kidney and is the target of thiazide diuretics, which are commonly prescribed to tre

96 Disease features are reversed by thiazide diuretics, which inhibit the Na-Cl cotransporte

97 ients except for NSAIDs, ACE inhibitors, and thiazide diuretics, which were more prevalent in black p

98 ive classes of antihypertensive medications, thiazide diuretics.

99 f action of SPIRO and a potential target for thiazide diuretics.

100 ressure 137/75 mm Hg [17/9]) who were not on thiazide diuretics.

101 1.43 to 3.91) compared with those prescribed thiazide diuretics.

102 d correction of physiologic abnormalities by thiazide diuretics.

103 al features of GS with a blunted response to thiazide diuretics.

104 onic anhydrases (CAs) confers the beneficial thiazide effect.

105 f the current study was to determine whether thiazides exert a direct bone-forming effect independent

106 Rats on high-fructose diets that are given thiazides exhibit potassium depletion and hyperuricemia.

107 As evidenced by the dictum to "use thiazides for most patients with uncomplicated hypertens

108 ion in risk for hip fracture associated with thiazide in many epidemiologic studies.

109 The density of receptors for thiazides in the rat DCT is known to be increased by adr

110 n addition to their antihypertensive effect, thiazides increase bone mineral density and reduce the p

111 s in fetal rat calvarial cells, we show that thiazides increase the formation of mineralized nodules,

112 However, thiazides induced antidiuresis and alkalinized the urine

113 NCC and the NDCBE/pendrin system may explain thiazide-induced hypokalemia in some patients.

114 widely used treatments for hypertension, but thiazide-induced hyponatremia (TIH), a clinically signif

115 int mutagenesis supports that the absence of thiazide inhibition is, at least in part, due to the sub

116 (NCC), which is the target of inhibition by thiazides, is located in close proximity to the chloride

117 lisinopril, or doxazosin was not superior to thiazide-like diuretic (chlorthalidone) in preventing co

118 Thiazide and thiazide-like diuretic agents are being increasingly use

119 Chlorthalidone is a potent, long-acting thiazide-like diuretic and should be used preferentially

120 was significantly better than thiazides and thiazide-like diuretics as a first-line therapy for any

121 Thiazide may have beneficial effects on bone mineral den

122 hypertensive drugs, our results suggest that thiazides may find a role in the prevention and treatmen

123 However, thiazide-mediated inhibition of NCC and consequent resto

124 f potassium supplements and allopurinol with thiazides might be helpful in the management of metaboli

125 However, <40% of patients treated with thiazide monotherapy achieve BP control.

126 ue-Dawley rats on (1) the density of the rat thiazide receptor (TZR), as quantitated by binding of (3

127 te solid phase may be the mechanism by which thiazides reduce CaOx stone formation.

128 The findings suggest that thiazide-related incident diabetes has less adverse long

129 n the upper normal to hypermagnesemic range, thiazide responsiveness was not blunted, and genetic ana

130 take, moderate-strength evidence showed that thiazides (RR, 0.52 [CI, 0.39 to 0.69]), citrates (RR, 0

131 (+) secretion via variable inhibition of the thiazide-sensistive NaCl cotransporter and the K(+) chan

132 Functional assessment of NCC by using thiazide-sensitive (22)Na(+) uptakes revealed that TPA c

133 studies implicate WNK4 in inhibition of both thiazide-sensitive co-transporter-mediated Na+ reabsorpt

134 A human homolog of rat thiazide-sensitive cotransporter was cloned and mapped t

135 rstanding of the molecular physiology of the thiazide-sensitive cotransporter, are strong evidence th

136 We recently described a novel thiazide-sensitive electroneutral NaCl transport mechani

137 However, aldosterone may also stimulate the thiazide-sensitive Na(+)-Cl(-) cotransporter (NCC).

138 The thiazide-sensitive Na(+)/Cl(-) cotransporter (NCC) is ac

139 ges include increases in the activity of the thiazide-sensitive Na(+)/Cl(-)-cotransporter (NCC).

140 Mutations in the gene encoding the thiazide-sensitive Na+-Cl- cotransporter (NCC) of the di

141 The Na+-H+ exchanger NHE3 and the thiazide-sensitive Na+-Cl- cotransporter NCC are the maj

142 e-sensitive Na+-K+-2Cl- cotransporters and a thiazide-sensitive Na+-Cl- cotransporter.

143 channel (ROMK), and total and phosphorylated thiazide-sensitive Na+Cl- cotransporter (NCC) levels wer

144 orylation sites, including serine-811 in the thiazide-sensitive Na-Cl co-transporter, NCC.

145 in increased whole-kidney abundances of the thiazide-sensitive Na-Cl co-transporter, the alpha-subun

146 " diuretic-sensitive Na-K-Cl cotransport and thiazide-sensitive Na-Cl cotransport.

147 Na-K-Cl cotransporter (NKCC or BSC) and the thiazide-sensitive Na-Cl cotransporter (NCC or TSC).

148 one increases expression and activity of the thiazide-sensitive Na-Cl cotransporter (NCC) and the epi

149 ) was shown to result from activation of the thiazide-sensitive Na-Cl cotransporter (NCC) by mutation

150 The thiazide-sensitive Na-Cl cotransporter (NCC) is the majo

151 sis revealed that the renal abundance of the thiazide-sensitive Na-Cl cotransporter (NCC) was profoun

152 esis that WNK kinases regulate the mammalian thiazide-sensitive Na-Cl cotransporter (NCC).

153 lting from loss of function mutations in the thiazide-sensitive Na-Cl cotransporter (NCCT) suggest th

154 alocorticoids regulate the expression of the thiazide-sensitive Na-Cl cotransporter (TSC), the chief

155 elationship between dietary Mg and the renal thiazide-sensitive Na-Cl cotransporter (TZR, measured by

156 CC2]), and the distal convoluted tubule (the thiazide-sensitive Na-Cl cotransporter [NCC]) in immunob

157 mRNA levels for the thiazide-sensitive Na-Cl cotransporter decreased by 57 a

158 Thus, the thiazide-sensitive Na-Cl cotransporter of the distal con

159 n's syndrome to the locus encoding the renal thiazide-sensitive Na-Cl cotransporter, and identify a w

160 rome, a disease caused by dysfunction of the thiazide-sensitive Na-Cl cotransporter.

161 ransporters in the distal nephron, including thiazide-sensitive Na-Cl cotransporters and ROMK channel

162 We showed previously that WNK4 downregulates thiazide-sensitive NaCl cotransporter (NCC) activity, an

163 renal distal convoluted tubule (DCT) by the thiazide-sensitive NaCl cotransporter (NCC) is a major d

164 The thiazide-sensitive NaCl cotransporter (NCC) is important

165 The thiazide-sensitive NaCl cotransporter (NCC) is the prima

166 The thiazide-sensitive NaCl cotransporter (NCC) of the renal

167 tenuating the cell surface expression of the thiazide-sensitive NaCl cotransporter (NCC).

168 The thiazide-sensitive NaCl cotransporter (NCC, SLC12A3) med

169 nt data suggest that sex hormones affect the thiazide-sensitive NaCl cotransporter (TSC) density or b

170 study the possible involvement of the renal thiazide-sensitive NaCl cotransporter gene in the syndro

171 ced urinary flow and reduced activity of the thiazide-sensitive NaCl cotransporter may support renal

172 Phosphorylation of the thiazide-sensitive NaCl cotransporter was consistently l

173 was no difference in the mRNA expressions of thiazide-sensitive NaCl cotransporter, epithelial Na cha

174 ulate the furosemide-sensitive NKCC2 and the thiazide-sensitive NCC, kidney-specific CCCs.

175 the two main sodium transport proteins, the thiazide-sensitive sodium chloride cotransporter (NCC) a

176 at occurs secondary to the inhibition of the thiazide-sensitive sodium chloride cotransporter (NCC) i

177 A T60M mutation in the thiazide-sensitive sodium chloride cotransporter (NCC) i

178 eported that tacrolimus stimulates the renal thiazide-sensitive sodium chloride cotransporter (NCC),

179 nal phosphorylation (encoded by WNK4) of the thiazide-sensitive sodium chloride cotransporter encoded

180 onstrated complete linkage between the human thiazide-sensitive sodium chloride cotransporter gene (N

181 t genes, Scnn1a, Scnn1b, and Scnn1g, and the thiazide-sensitive sodium chloride cotransporter gene, S

182 cient mice, which are unable to activate the thiazide-sensitive sodium chloride cotransporter NCC (en

183 The thiazide-sensitive sodium chloride cotransporter, NCC, i

184 is a potent driver of hypertension, and the thiazide-sensitive sodium-chloride cotransporter (NCC) h

185 stering the view that hyperactivation of the thiazide-sensitive sodium-chloride cotransporter (NCC) i

186 t sodium-chloride co-transporter, NKCC2, and thiazide-sensitive sodium-chloride cotransporter, NCC, i

187 expression and NCC activity, as measured by thiazide-sensitive, chloride-dependent (22)Na uptake, we

188 distal convoluted tubule and indicates that thiazides should be useful in reducing the risk of kidne

189 Because NCC and NDCBE are both thiazide targets, the combined inhibition of NCC and the

190 For calcium channel blockers and thiazides, the matched odds ratios were 4.21 (95% CI, 1.

191 CA-SPAK mice displayed thiazide-treatable hypertension and hyperkalemia, concur

192 However, <50% of thiazide-treated patients achieve blood pressure (BP) co

193 in children may be improved with citrate or thiazide treatment.

194 eased blood pressure, which were reversed by thiazide treatment.

195 tic agents that impair this mechanism (e.g., thiazide-type diuretic agents and mineralocorticoid rece

196 eceptor blocker irbesartan, but not with the thiazide-type diuretic chlorthalidone, restored sympatho

197 eceptor blocker, calcium channel blocker, or thiazide-type diuretic in the nonblack hypertensive popu

198 with diabetes, a calcium channel blocker or thiazide-type diuretic is recommended as initial therapy

199 oop diuretic resistance is the addition of a thiazide-type diuretic to produce diuretic synergy via "

200 ith 2 agents, 1 of which usually should be a thiazide-type diuretic; and (7) The most effective thera

201 Thiazide-type diuretics are associated with an increased

202 nation diuretic therapy using any of several thiazide-type diuretics can more than double daily urine

203 lifestyle modifications to prevent CVD; (4) Thiazide-type diuretics should be used in drug treatment

204 the investigators' original conclusion that thiazide-type diuretics should remain the preferred firs

205 ctivity and causes insulin resistance during thiazide usage.

206 n 140/90 mm Hg (OR, 1.0 [95% CI, 0.92-1.2]); thiazide use (OR, 1.0 [95% CI, 0.8-1.3]); atheroscleroti

207 The prevalence of thiazide use was higher among the glaucoma cases than am

208 A protective effect for current thiazide use was observed (OR = 0.53, CI = 0.31-0.90), a

209 was used to adjust for age, body mass index, thiazide use, and dietary factors.

210 ke of calcium, animal protein and potassium, thiazide use, geographic region, profession, and total f

211 either citrate nor allopurinol combined with thiazide was superior to thiazide alone.

212 nd controls for calcium channel blockers and thiazides was noted.

213 tion of calcium channel blockers, as well as thiazides, with CEEA in the United States.